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Anti-inflammatory activity of coptisine free base in mice through inhibition of NF-κB and MAPK signaling pathways.
Eur J Pharmacol. 2017 Sep 15; 811:222-231.EJ

Abstract

Coptisine is one of the main constituents of Coptis chinensis which has been widely used for the remedy of inflammatory disorders. Although the biological activities of coptisine have been well known, the pharmacological properties of its free base have seldomly been elucidated thus far. The aim of this study was to investigate the potential anti-inflammatory properties of coptisine free base (CFB, 8-hydroxy-7,8-dihydrocoptisine) on three animal models, namely xylene-induced ear edema, acetic acid-induced vascular permeability and carrageenan-induced paw edema. The results exhibited that CFB exerted a dose-dependent suppression on ear edema induced by xylene, significantly mitigated the aggravation of vascular permeability caused by acetic acid and paw edema induced by carrageenan. Additionally, CFB significantly suppressed the productions of interleukin-1β (IL-1β), interleukin-6 (IL-6), prostaglandinE2 (PGE2) and tumor necrosis factor (TNF-α) in the drug-treated groups as compared with the vehicle group after treatment with carrageenan. Signaling events of nuclear factor-κB (NF-κB) translocation, such as p-IKKα, p-IKKβ, p-IκBα and p65 (nucleus) were significantly inactivated, while inhibitor of nuclear factor κBα (IκBα) and p65 (cytosolic) were markedly up-regulated by CFB. Furthermore, CFB also significantly suppressed the mitogen-activated protein kinase (MAPK) pathway by blocking the phosphorylation of p-p38 (phospho-p38 mitogen-activated protein kinases) and p-JNK (phospho-c-jun N-terminal kinase) but not p-ERK (phospho-extracellular signal-regulated kinase). Hence, CFB efficiently prevented inflammation, at least partially, via inhibition of NF-κB and MAPK pathways. These findings provided a pioneering pharmacological basis for the anti-inflammatory effect of CFB and suggested CFB might be a potential candidate for the therapy of inflammatory disorders.

Authors+Show Affiliations

The First Affiliated Hospital of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou 510405, People's Republic of China.Guangdong Provincial Key Laboratory of New Drug Development and Research of Chinese Medicine, School of Chinese Materia Medica, Guangzhou University of Chinese Medicine, Guangzhou 510006, People's Republic of China.Guangdong Provincial Key Laboratory of New Drug Development and Research of Chinese Medicine, School of Chinese Materia Medica, Guangzhou University of Chinese Medicine, Guangzhou 510006, People's Republic of China.Guangdong Provincial Key Laboratory of New Drug Development and Research of Chinese Medicine, School of Chinese Materia Medica, Guangzhou University of Chinese Medicine, Guangzhou 510006, People's Republic of China.Guangdong Provincial Key Laboratory of New Drug Development and Research of Chinese Medicine, School of Chinese Materia Medica, Guangzhou University of Chinese Medicine, Guangzhou 510006, People's Republic of China.The First Affiliated Hospital of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou 510405, People's Republic of China.Guangdong Provincial Key Laboratory of New Drug Development and Research of Chinese Medicine, School of Chinese Materia Medica, Guangzhou University of Chinese Medicine, Guangzhou 510006, People's Republic of China.Guangdong Provincial Key Laboratory of New Drug Development and Research of Chinese Medicine, School of Chinese Materia Medica, Guangzhou University of Chinese Medicine, Guangzhou 510006, People's Republic of China.Guangdong Provincial Key Laboratory of Clinical Research on Traditional Chinese Medicine Syndrome, The Second Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou 510120, People's Republic of China.Guangdong Provincial Key Laboratory of New Drug Development and Research of Chinese Medicine, School of Chinese Materia Medica, Guangzhou University of Chinese Medicine, Guangzhou 510006, People's Republic of China; Dongguan Mathematical Engineering Academy of Chinese Medicine, Guangzhou University of Chinese Medicine, Dongguan 523808, People's Republic of China.Guangdong Provincial Key Laboratory of Clinical Research on Traditional Chinese Medicine Syndrome, The Second Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou 510120, People's Republic of China. Electronic address: xiejianhui888@hotmail.com.The First Affiliated Hospital of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou 510405, People's Republic of China. Electronic address: gancaozhf@126.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28648405

Citation

Chen, Han-Bin, et al. "Anti-inflammatory Activity of Coptisine Free Base in Mice Through Inhibition of NF-κB and MAPK Signaling Pathways." European Journal of Pharmacology, vol. 811, 2017, pp. 222-231.
Chen HB, Luo CD, Liang JL, et al. Anti-inflammatory activity of coptisine free base in mice through inhibition of NF-κB and MAPK signaling pathways. Eur J Pharmacol. 2017;811:222-231.
Chen, H. B., Luo, C. D., Liang, J. L., Zhang, Z. B., Lin, G. S., Wu, J. Z., Li, C. L., Tan, L. H., Yang, X. B., Su, Z. R., Xie, J. H., & Zeng, H. F. (2017). Anti-inflammatory activity of coptisine free base in mice through inhibition of NF-κB and MAPK signaling pathways. European Journal of Pharmacology, 811, 222-231. https://doi.org/10.1016/j.ejphar.2017.06.027
Chen HB, et al. Anti-inflammatory Activity of Coptisine Free Base in Mice Through Inhibition of NF-κB and MAPK Signaling Pathways. Eur J Pharmacol. 2017 Sep 15;811:222-231. PubMed PMID: 28648405.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Anti-inflammatory activity of coptisine free base in mice through inhibition of NF-κB and MAPK signaling pathways. AU - Chen,Han-Bin, AU - Luo,Chao-Dan, AU - Liang,Jia-Li, AU - Zhang,Zhen-Biao, AU - Lin,Guo-Sheng, AU - Wu,Jia-Zhen, AU - Li,Cai-Lan, AU - Tan,Li-Hua, AU - Yang,Xiao-Bo, AU - Su,Zi-Ren, AU - Xie,Jian-Hui, AU - Zeng,Hui-Fang, Y1 - 2017/06/23/ PY - 2017/02/11/received PY - 2017/06/12/revised PY - 2017/06/21/accepted PY - 2017/6/27/pubmed PY - 2018/5/31/medline PY - 2017/6/27/entrez KW - Anti-inflammation KW - Berberine KW - Berberine (PubChem CID: 2353) KW - Carrageenan (PubChem CID: 11966249) KW - Coptis chinensis KW - Coptisine (PubChem CID: 72321) KW - Coptisine free base KW - Diethyl ether (PubChem CID: 3283) KW - Dimethyl sulfoxide-d(6) (PubChem CID: 75151) KW - Evans Blue (PubChem CID: 5359386) KW - Indomethacin (PubChem CID: 3715) KW - MAPK KW - NF-κB KW - NaOH (PubChem CID: 14798) KW - Tween-80 (PubChem CID: 5281955) KW - Xylene (PubChem CID: 7809) SP - 222 EP - 231 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 811 N2 - Coptisine is one of the main constituents of Coptis chinensis which has been widely used for the remedy of inflammatory disorders. Although the biological activities of coptisine have been well known, the pharmacological properties of its free base have seldomly been elucidated thus far. The aim of this study was to investigate the potential anti-inflammatory properties of coptisine free base (CFB, 8-hydroxy-7,8-dihydrocoptisine) on three animal models, namely xylene-induced ear edema, acetic acid-induced vascular permeability and carrageenan-induced paw edema. The results exhibited that CFB exerted a dose-dependent suppression on ear edema induced by xylene, significantly mitigated the aggravation of vascular permeability caused by acetic acid and paw edema induced by carrageenan. Additionally, CFB significantly suppressed the productions of interleukin-1β (IL-1β), interleukin-6 (IL-6), prostaglandinE2 (PGE2) and tumor necrosis factor (TNF-α) in the drug-treated groups as compared with the vehicle group after treatment with carrageenan. Signaling events of nuclear factor-κB (NF-κB) translocation, such as p-IKKα, p-IKKβ, p-IκBα and p65 (nucleus) were significantly inactivated, while inhibitor of nuclear factor κBα (IκBα) and p65 (cytosolic) were markedly up-regulated by CFB. Furthermore, CFB also significantly suppressed the mitogen-activated protein kinase (MAPK) pathway by blocking the phosphorylation of p-p38 (phospho-p38 mitogen-activated protein kinases) and p-JNK (phospho-c-jun N-terminal kinase) but not p-ERK (phospho-extracellular signal-regulated kinase). Hence, CFB efficiently prevented inflammation, at least partially, via inhibition of NF-κB and MAPK pathways. These findings provided a pioneering pharmacological basis for the anti-inflammatory effect of CFB and suggested CFB might be a potential candidate for the therapy of inflammatory disorders. SN - 1879-0712 UR - https://www.unboundmedicine.com/medline/citation/28648405/Anti_inflammatory_activity_of_coptisine_free_base_in_mice_through_inhibition_of_NF_κB_and_MAPK_signaling_pathways_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(17)30434-X DB - PRIME DP - Unbound Medicine ER -